Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 1 de 1
Filter
Add more filters










Database
Language
Publication year range
1.
Oncol Rep ; 44(4): 1343-1354, 2020 10.
Article in English | MEDLINE | ID: mdl-32945477

ABSTRACT

Increasing research has demonstrated that lncRNAs participate in the development of multiple cancer types. However, the role of TTN­AS1 in endometrial cancer (EC) remains unknown. The present study aimed to explore the function of titin­antisense RNA1 (TTN­AS1) in EC progression and the underlying mechanisms. qRT­PCR was performed to assess the TTN­AS1 expression patterns in EC tissues and cell lines. Loss of function experiments were carried out to estimate the effects of TTN­AS1 on EC cell proliferation, migration and invasion. To reveal the underlying mechanisms, informatics tools were used to predict the targets. Rescue experiments were performed to investigate the TTN­AS1­regulated miR­376a­3p/pumilio homolog 2 (PUM2) axis involved. The results of the present study revealed that TTN­AS1 was highly expressed in both EC tissues and cell lines, and TTN­AS1 knockdown inhibited EC cell proliferation, migration and invasion. With respect to the mechanisms, miR­376a­3p was revealed to be targeted by TTN­AS1, and reversed the effects on EC development induced by TTN­AS1. In addition, PUM2 was positively regulated by TTN­AS1, and miR­376a­3p mediated the regulation between them. Furtherly, in vivo experiments confirmed the results. Collectively, TTN­AS1 enhanced EC cell proliferation and metastasis by targeting the miR­376a­3p/PUM2 axis, which may shed light on EC diagnosis and treatment.


Subject(s)
Connectin/genetics , Endometrial Neoplasms/genetics , MicroRNAs/genetics , RNA, Long Noncoding/genetics , RNA-Binding Proteins/genetics , Apoptosis/genetics , Cell Line, Tumor , Cell Movement/genetics , Cell Proliferation/genetics , Endometrial Neoplasms/pathology , Female , Gene Expression Regulation, Neoplastic/genetics , Humans
SELECTION OF CITATIONS
SEARCH DETAIL
...